摘要
本工作在细胞水平研究生长抑素保护胰岛细胞,防止链佐霉素损伤的可能机制,结果表明,生长抑素很可能通过抑制链霉素进入胰岛细胞,进而阻止细胞内尼克酰胺腺嘌呤二核苷酸(NAD)的耗竭而实现其保护作用的。
Examination was performed to study the mechanism concerning the protective effect of somatostatin on isolated islet cells damaged by streptozotocin (STZ). It was found that somatosta-tin (0.1 μg/ml) could hinder the incorporation of 3H-STZ into the islet cells, therefore the depletion of NAD in islet cells induced by STZ was prevented. The incorporation percentage was decreased from 100 + 8.9% in damaged group to 44.90+7.09% in protected group ( p<0.001); the NAD content was increased from 0.190 ± 0.082 pmol/105 cell in damaged group to 0.442± 0.071 pmol/105 cell in protected group (p<0.05).The results indicate that the inhibition of the intracellular entry of STZ might be one of the protective mechanisms of somatostatin on pancreatic islet cells.
出处
《北京医科大学学报》
CSCD
1989年第3期202-204,共3页
Journal of Peking University(Health Sciences)
关键词
生长抑素
链佐霉素
胰岛B细胞
Somatostatin Streptozotocin Pancreatic islet cell